There is a correlation between age-related hearing loss and cognitive decline. Is this because similar mechanisms of cell and tissue damage disrupt both the function of the brain and nerve cells in the ears, or is this because hearing is important in the ongoing operation of the brain? Supporting evidence exists for both options. Here, researchers discuss ways in which loss of hearing might disrupt brain function.

Hearing loss in midlife has been estimated to account for 9% of cases of dementia. Acquired hearing loss is most commonly caused by cochlear damage, while dementia is due to cortical degeneration that typically begins in multimodal cortex. This immediately begs the question of how the two are linked. This is a crucial question from a theoretical perspective, as there are multiple biological and psychological pathways that may link peripheral auditory function to broad-based cortical changes associated with dementia. It also has critical practical implications because while it is difficult, if not impossible, to remediate cortical degradation, hearing loss is widely treatable with hearing aids or cochlear implants. Thus, an understanding of the mechanisms linking the two could have wide-ranging public health importance.

There are a number of possible mechanisms for the relationship between hearing loss and dementia. A first possible mechanism is common pathology affecting the cochlea and ascending auditory pathway (causing hearing loss) and the cortex (causing dementia). Alzheimer’s disease (AD)-related pathology has been observed in the retina, but it is not well established as occurring in the cochlea. Transgenic mouse models of AD suggest that AD may be associated with cochlear pathology and hearing loss, but the loss is early onset, unlike the midlife impairment in humans. Vascular pathology can also occur in the cochlea, and this is one of the factors implicated in typical acquired hearing loss. It can also affect the ascending auditory pathway and auditory cortex. Vascular mechanisms are therefore potential contributors to the hearing loss associated with cases of vascular dementia.

A second possible mechanism is that hearing loss leads to the decreased stimulation of cognitive processing. The idea is that auditory deprivation creates an impoverished environment, particularly with the diminishment of speech and language input, that negatively affects brain structure and function. This change in brain structure and function is a risk factor for the subsequent development of dementia. A variety of lines of evidence suggest that listening experience may have a direct impact on the human brain. In parallel to the enriched environment studies with mice, the active listening experience of musicians is associated with positive effects on the structure of auditory cortex and the hippocampus and functional changes in the hippocampus. Piano tuners, expert listeners who spend large amounts of time carrying out a highly specialized form of selective listening, demonstrate hippocampal structural correlates of that experience.

A third mechanism is based on the idea that people with hearing impairment use greater cognitive resources for listening, making these resources unavailable for other aspects of higher cognition when they are “occupied” during listening. “Resources” refers here to the means for cognitive tasks such as attention, working memory, or language processing. There is debate about how cognitive resources are allocated, and the corresponding neural bases. With respect to working memory, for example, there is a question about the extent to which resources may be specifically allocated to objects or represent a distributed resource. Further debate concerns the extent to which working memory resources reflect neuronal or synaptic mechanisms, or both. What is important here, however, is that there is a fixed capacity for many general cognitive operations. These resources may be absorbed when listening becomes challenging, reducing their availability for other aspects of cognition.

A fourth possible explanation focuses on auditory cognitive mechanisms in the medial temporal lobe (MTL) that may be specifically linked to AD pathology in the same region. Although MTL structures are not classically regarded as part of the auditory system, animal models support their role in auditory processing. This mechanism starts from the same idea as the prior mechanism, that hearing loss alters cortical activity, including in the MTL. The critical difference is the incorporation of an interaction between that altered activity and AD pathology. The AD pathology that best correlates with the cognitive phenotype is neurofibrillary change related to tau pathology. The earliest neurofibrillary changes in typical AD are found in MTL structures, particularly the perirhinal cortex, which has a strong functional relationship to the hippocampus. This raises the possibility of an interaction between this pathological process and changes in neuronal activity in MTL structures that occur in hearing impaired individuals.